BARRETT’S ESOPHAGUS
GENERAL THORACIC SURGERY
CHAPTER 141
HISTORY
• Norman Barrett(1950) — congenitally short esophagus with an intrathoracic stomach.
• Allison and Johnstone (1953) and Lortat-Jacob (1957)—an abnormal columnar epithelium lining the distal esophagus—Barrett’s esophagus.
• Adopt by Barrett himself—acquired, not congenital disorder.
Definition
• Normal distal esophagus — may display short cephalad extention of columnar epithelium above the gastroesophageal junction.
• An endoscopic diagnosis.• Circumferential, columnar epithelial lining
of distal esophagus extending at least 3 cm above the gastroesophageal junction.
TYPE
• Gastric fundic type resembling stomach epithelium.
• Junctional epithelium resembling gastric cardia.• Intestinal glandular epithelium characterized by
goblet cell. • The intestinalized epithelium is most common and
importannt histologic type — predisposing patient to the develop the adenocarcinoma of esophagus.
Pathogenesis
• Gastroesophageal reflux — leads to destruction of the normal squamous lining of esophagus, and allow subsequent cephalad migration of columnar gastric lining to re-epithelized the injured area.
• Alkaline reflux — also involved, particularly in developing complication.
• Chemotherapy — as cyclophosphamide, methotrexate, 5-FU.
• Congenital — fetal development the columnar epithelium is replaced by squamous epithelium, island of columnar epithelium persist, usually at proximal esophagus, associated with GER.
Prevalence
• 2% of patient undergoing panendoscopy.
• 44 % patient of peptic stricture with Barrett’s esophagus.
• 27/100000.
• Autopsy 376/100000.
• Most barrett’s esophagus are asymptomatic.
Clinical feature
• Asymptomatic.
• GER and complication.
• Heartburn, regurgitation.
• Dysphagia from stricture or carcinoma.
• Tobacco and alcohol use.
Radiology
• Difficult to diagnose by radiography.
• Sliding hiatal hernia with esophagitis.
Endoscopy
• Essential to confirm diagnosis. • Squamous epithelium is more smooth, pale, the
columnar epithelium is more granular, reddish. and often contain signs of reflux injury.
• Endoscopic biopsy should be performed in all suspected cases, to confirm the search for dysplasia.
• Methylene blue associated stain area of epithelial dysplasia to guide biopsies.
Esophageal manometry and pH testing
• Diminished lower esophageal sphincter pressure, poorer esophageal acid clearance more frequent esophageal acid exposure, time of distal esophageal pH less than 4 is 15-39%.
• Twice as high as patient with esophagitis without Barrett’s esophagus, 10 fold higher than normal.
Biomarkers
• Alteration in DNA content.
• p53 mutation.
• p27 inactived.
Complication.
Ulceration and stricture
• More in patient with Barrett’s esophagus ( 10-15% ) than in GER.
• Ulcer penetrate the columnar epithelium, like the gastric ulcer, acid-peptic erosion, alkaline reflux.
• s/s — bleeding, pain, obstruction ( 30% ) , perforation, irondeficiency anemia, dysphagia, perforation into pleural space, lung, pericardium.
• Stricture always at squamocolumnar junction.
Dysplasia
• Low and high grade.
• Loss pf nuclear polarity, hyperchromatism, nuclear enlargement, stratification, pleomorphism, abnormal mitoses.
• Distinguish high and low grade is difficult.
Adenocarcinoma
• Distinguish adenocarcinomna in Barrett’s esophagus from carcinoma of cardia is difficult.
• 30-125 times the risk of normal population.
• 1 case per 100 patient-year, annual risk 1%.
Treatment
Benign Barrett’s esophagus
• Asymptomatic and uncomplication not require treatment.
• Medical treatment of GER infrequently regression the Barrett’s epithelium, or only partial, island or underlying columnar epithelium, still at risk for dysplasia.
• Treatment use the same guideline for GER. • Antireflux surgery not lessen risk of malignant
degeneration of Barrett’s epithelium.
Stricture
• Periodic dilation, weight loss, elevated head of bed, dietary modification.
• Transabdominal Nissen fundoplication coupled with intraoperative dilation.
• Left thoracotomy for complete esophageal mobilization to permit lengthening procedure as Collis’ gastroplasty if any display evidence of esophageal shortening.
Barrett’s ulcer
• Most heal with medical therapy — H2-blocker, PPI, prolong therapy exceeding 8 weeks, response rate 85%.
• Recurrence common.
• If ulcer fail to heal after medical treatment 4 months, the antireflux surgery — Collis’-Belsey repair, Collis’-Nissen fundoplication.
Low-grade dysplasia
• Early signal that carcinoma may develop.
• Most low grade not progress to high grade or invasive carcinoma.
• Medical therapy is recommended even in absence of symptoms.
• More frequent endoscopic surveillance to ensure prompt detection.
High-grade dysplasia
• Indication of esophagectomy. • 22-73% chance unsuspected invasive
carcinoma. • Esophagogastrectomy. • 100% cure rate patient without invasive
tumor. • Thermal laser, photodynamic therapy —
long term efficacy and cost-effectiveness unknown.
Adenocarcinoma
• Esophagogastrectomy.
• Higher respectability — 94-100%.
• Long term survival similar — 20% in 5-year.